Benign prostatic hyperplasia (BPH) and prostatitis: prevalence of painful ejaculation in men with clinical BPH.
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OBJECTIVE: Prostate cancer (PRCa) is one of the most common causes of cancer death in men and determinants of PRCa risk remain largely unidentified. Benign prostatic hyperplasia (BPH) is found in the majority of ageing men and has been associated with PRCa. Many candidate genes have been suggested to be involved in PRCa, such as those that are central to cellular growth and differentiation in the prostate gland. The vitamin D receptor (VDR) and HER-2 protooncogene have been shown to be involved in the regulation of cell proliferation and differentiation in prostate cells. Genetic variations of these genes could be useful to detect BPH patients that have a higher risk of developing PRCa. This study used a case-control design to assess the predictive value of 3 polymorphisms in VDR (TaqI and FokI) and HER-2 (Val655Ile) to determine the risk of developing PRCa in patients with BPH. METHODS: Polymorphisms were detected by RFLP analysis. The study evaluated 28 patients who presented with PRCa at least 6 years after the diagnosis of BPH and 56 matched patients with BPH who did not progress to PRCa over a comparable period. The study was carried out in University of Aberdeen, Foresterhill, Aberdeen, United Kingdom in the year 2002. RESULTS: Among the case group, 89% had a TT TaqI genotype, whereas 57% of control had this genotype (odds ratio [OR] = 5.16, 95% confidence interval [CI] = 1.46-18.22). A similar pattern was seen for the FokI genotype, although this was not statistically significant (OR = 2.33, 95% CI = 0.86-6.29). The frequency of the HER-2 Ile/Ile genotype was higher in cases (79%) compared to control subjects (66%), although this was not statistically significant (OR = 1.94, 95% CI = 0.67-5.63). CONCLUSION: This study shows that the VDR TaqI polymorphism is associated with a group of men with BPH who are at an increase risk of PRCa, providing a potential tool to assist prediction strategies for this important disease.
PURPOSE: Accurately estimating transition zone volume is important for the medical or surgical management of symptomatic benign prostatic hyperplasia and determination of prostate specific antigen density of the transition zone. We evaluated whether preoperative transrectal ultrasound measurements of the transition zone predict enucleated adenoma weight. MATERIALS AND METHODS: We measured transition zone volume preoperatively using transrectal ultrasound and the prolate ellipsoid method in 50 patients with presumed benign prostatic hyperplasia who underwent suprapubic prostatectomy. Transition zone volume corresponds to the adenoma. Enucleated adenoma weight was then correlated with preoperatively determined transition zone volume. RESULTS: As measured by transrectal ultrasound, mean transition zone volume plus or minus standard deviation was 80.88 +/- 37.42 cc (range 31 to 200). Mean enucleated adenoma weight was 68.70 +/- 36.26 gm. (range 18 to 180). There was a statistically significant correlation of estimated transrectal ultrasound volume of the transition zone with enucleated prostate adenoma weight (r = 0.95, p <0.001). However, when prostate adenoma weight was determined using the formula, prostate adenoma weight = -6.00 + 0.92 x transition zone volume, we noted a significant difference in mean prostate adenoma weight and mean transition zone volume (p <0.001). Since the regression coefficient of transition zone volume was significantly different from 1, we identified no agreement of prostate adenoma weight with estimated transrectal ultrasound volume of the transition zone. CONCLUSIONS: These data reveal a significant difference in mean prostatic adenoma weight and mean transition zone volume. Although transition zone volume measurements are well described, clear agreements on such measurements should be obtained to determine transition zone volume more precisely.
Prostate-specific antigen (PSA), as measured in peripheral blood, is currently the most widely used marker for the assessment of tumor burden in the longitudinal study of patients with carcinoma of the prostate (PCA). Studies from other laboratories have led to the conclusion that a given volume of PCA causes a much higher level of PSA in the peripheral circulation of patients than a similar volume of prostate without carcinoma. We have evaluated PSA in the resected tissues immunohistochemically and in extracts of PCA and of prostates resected because of benign prostatic hyperplasia (BPH) with an enzyme-linked immunosorbent assay. Immunohistochemical results were less quantitative than but consistent with the results of the ELISA of tissue extracts. Immunohistochemically, there was considerable heterogeneity in the expression of PSA by both PCA and BPH both within and among prostatic tissues from different patients. While the levels of expression of PSA in these tissues overlap broadly, PSA is expressed at a lower level in PCA than in BPH when PSA is expressed as a function of wet weight of tissue (p = 0.0095), wet weight of tissue/% epithelium (p less than 0.0001), protein extracted from the tissue (p = 0.0039), or protein extracted/% epithelium (p less than 0.0001).
Benign prostate hyperplasia (BPH) is a common disease in elderly men. Although it is a non-malignant disease, it has a significant detrimental impact on the quality of life in patients with late-stage disease. Owing to the lack of specific markers, diagnosis of early-stage BPH has been proven unsuccessful. Recently, using two-dimensional electrophoresis, we identified a group of prostatic secretory proteins that are specifically produced by BPH cells (Xu et al., Electrophoresis 2003; 24: 1311). In this study, we investigated the potential diagnostic value of one of the secretory proteins, alphas1-Casein, in BPH by inmmunohistological staining of normal, BPH and prostate cancer tissues. We found that 90% (20 out of 22) of BPH tissues showed moderate to strong alphas1-Casein protein expression whereas none of the normal tissues (0 out of 10) and less than 10% of the prostate cancer tissues (3 out of 30) showed similar staining intensity. Our results suggest that alphas1-Casein may be a potential biomarker for early identification of BPH patients.
PURPOSE: Benign prostatic hyperplasia is common among men who may be candidates for prostate cancer screening using prostate-specific antigen (PSA) testing. Patterns of PSA testing among men with evidence of benign prostatic hyperplasia have not been studied. METHODS: We examined the prevalence and correlates of a self-reported history of PSA testing. In 1994, 33,028 US health professionals without prostate cancer aged 47 to 85 years provided information on prior PSA testing, lower urinary tract symptoms characteristic of benign prostatic hyperplasia, history of prostatectomy, and prostate cancer risk factors. In 1995, a subset of 7,070 men provided additional information on diagnosis and treatment of benign prostatic hyperplasia. RESULTS: From 39% of men in their 50s to 53% of men in their 80s reported PSA testing in the prior year (P <0.0001 for trend with age). Men were more likely to report PSA testing if they had lower urinary tract symptoms characteristic of benign prostatic hyperplasia (age-adjusted odds ratio for severe symptoms 2.2, 95% confidence interval 1.8 to 2.6), a prior history of prostatectomy (age-adjusted odds ratio 1.1, 95% confidence interval 1.02 to 1.2), or a physician diagnosis of benign prostatic hyperplasia (odds ratio 1.9, 95% confidence interval 1.7 to 2.2; adjusted for age, signs or symptoms of benign prostatic hyperplasia, and prostate cancer risk factors). CONCLUSIONS: These US health professionals reported preferential use of PSA testing among men least likely to benefit from early cancer detection (older men) and among men most likely to have a false-positive PSA result (men with benign prostatic hyperplasia). Physician and patient education are needed to promote more rational and selective use of this screening test.
Prostate-specific antigen (PSA) is the most useful tumor marker for diagnosis and monitoring of prostate cancer (CaP). Recently, we developed a specific immunoassay for human kallikrein 11 (hK11), one of the kallikrein gene family members, and found that hK11 was highly expressed in prostatic tissue and could be detected in seminal plasma (E. P. Diamandis et al., Cancer Res., 62: 295-300, 2002). The aim of this study was to investigate whether serum hK11 levels could be used to discriminate CaP from benign prostatic hyperplasia (BPH). We analyzed for hK11, total PSA, and percentage of free PSA, 150 serum samples from men with histologically confirmed BPH (n = 64) or CaP (n = 86). Total and free PSA levels were measured by the Immulite PSA assay, and hK11 levels were measured by our previously published immunofluorometric assay. Serum hK11 levels and the hK11:total PSA ratio were both significantly lower in CaP patients than in BPH patients. In the subgroup of patients with percentage of free PSA less than 20, an additional 54% of BPH patients could have avoided biopsies by using the hK11:total PSA ratio. Receiver operating characteristic (ROC) curve analysis demonstrated that the hK11:total PSA ratio [area under the curve (AUC), 0.83] and percentage of free PSA (AUC, 0.83) were much stronger predictors of CaP than total PSA (AUC, 0.69). These preliminary data suggest that the hK11:total PSA ratio could be a useful tumor marker for CaP and could be combined with percentage of PSA to further reduce the number of unnecessary prostatic biopsies.
Benign prostatic hyperplasia (BPH) is an extremely common condition and represents a major health issue in terms of patient numbers and treatment cost. Traditionally, the choice of treatment has been between watchful waiting and surgery, however, the side effects of surgery lead to reluctance for treatment in many men, other than those with severe symptoms and complications. In the last 2 decades there has been a rapid expansion in the number of treatments being offered and the number of patients submitting to novel therapies. Medical management has evolved to achieve a central role in the management of BPH. Heat based treatments are also being investigated with considerable interest. Transrectal high intensity focused ultrasound (HIFU) is one such treatment, which allows radiation-free treatment, without the need for intra-urethral manipulation. Imaging can be performed during treatment and treatment results in symptomatic improvement, which is retained with medium-term follow-up. It involves a brief hospital stay and post-operative complications are few. The use of HIFU has also been extended to the treatment of renal, prostatic and bladder tumours and the results in these areas suggest further expansion of its role in urological practice.
Benign prostatic hyperplasia (BPH) is an important cause of lower urinary tract symptoms (LUTS). However, many other causes, including smooth muscle dysfunction and neurological factors may contribute to these symptoms, and accurate diagnosis is imperative before invasive treatments are chosen. Careful recording of symptoms, giving emphasis on how they interfere with the patient's quality of life, as well as the use of properly selected tests, constitutes the mainstay of making a correct diagnosis. Men with mild or moderate symptoms not experiencing complications are ideal candidates for medical treatment. For the rest with persistent symptoms or complications such as infection, bleeding, chronic retention or renal impairment further investigation and more invasive forms of treatment need to be considered. We review the patho-physiology of the disease, and current approaches and management of this common problem.
Prostate-specific antigen (PSA), the main marker for prostate cancer (PCa), is released from the prostate into the blood stream at nanogram level and may increase in PCa and nonmalignant disease such as benign prostate hyperplasia (BPH). More recently, advantage was taken of PSA's ability to bind to protease inhibitors in serum in order to improve discrimination between PCa and BPH, using the free PSA to total PSA ratio. The understanding of this phenomenon at molecular level, which is still unknown, may promise new improvements in the field of diagnostics. For this purpose, we determined the pattern of PSA forms in PCa and BPH sera, using the high resolving power of two-dimensional electrophoresis (2-DE) in conjunction with the high sensitivity of chemiluminescence detection. Serum PSA differs drastically from seminal PSA: apart from complexed forms, serum PSA shows few cleaved forms. Moreover, 2-DE patterns from PCa are relatively homogeneous, whereas patterns from BPH may in some cases present a higher proportion of cleaved forms and in other cases present slightly more basic spots. We therefore demonstrated, for the first time, that an increase in the free to total PSA ratio in BPH cases may be due to cleaved PSA forms (which are enzymatically inactive and unable to bind inhibitors), or possibly related to basic free PSA, which may represent the zymogen forms.
Benign prostatic hyperplasia (BPH) is a disease affecting the majority of aging men; 90% of men develop histological BPH by the time they reach their eighties. BPH can lead to bothersome lower urinary tract symptoms (LUTS), which may reduce quality of life. Many patients fail current treatment options and may progress to surgical intervention. Furthermore, diagnosis is reliant on symptom questionnaires and the cause of LUTS can be difficult to distinguish. Currently, BPH can only be definitively diagnosed through histological analysis of prostate tissue, which is not the standard of care. The resulting lack of clinical tissue samples is a major limitation in investigating disease pathology. Improved understanding of disease development and progression, along with objective biomarkers of disease, is needed for BPH. This investigation uses mass spectrometry (MS)-based proteomics and glycoproteomics to compare healthy prostate tissue with prostate tissue affected by BPH to address this gap in knowledge. By integrating proteomics and glycoproteomics, we identified 206 proteins and 44 glycopeptides that were significantly altered between BPH and control samples. These findings provide deeper insight into disease-associated pathways and may facilitate the identification of clinically relevant targets for further investigation.
The levels of immunoreactive prostatic inhibin-like peptide (PIP), having follicle-stimulating hormone suppressing properties, were estimated in the sera and urine samples of patients with benign prostatic hyperplasia (BPH) and prostatic carcinoma (PC) as compared to age-matched controls. Significantly elevated serum PIP levels in BPH (107.8 +/- 19 ng/ml) and PC (88.7 +/- 9 ng/ml) patients were observed as compared to those in control men (10.2 +/- 1 ng/ml). Unlike serum, in urine high levels of PIP in BPH (294 +/- 49 micrograms/24 h) and extremely low levels in PC (23.6 +/- 5 micrograms/24 h) patients were seen as compared to control values (137.6 +/- 10 micrograms/24 h). Furthermore, striking differences were observed between the urinary PIP levels of BPH and PC patients. The results of the present investigation thus indicate the possible use of urinary PIP as a biological marker for prostate cancer.
OBJECTIVE: To determine whether the ratio of PSA and prostate volume provides additional useful information for the discrimination of benign prostatic hyperplasia from prostatic carcinoma. PATIENTS AND METHODS: Since 1989, a prospective study has been in progress involving 229 patients (49 with locally confined prostatic carcinoma, 180 with benign prostatic hyperplasia) to establish whether the ratio of prostate-specific antigen (PSA) and prostate volume, determined by transrectal ultrasound (longitudinal x anterior-posterior x transverse diameter x 0.52), allows a better differentiation than the absolute PSA values. RESULTS: In this population of patients with prostatic disease, the positive predictive value for diagnosis of a prostatic carcinoma was 26% with an absolute PSA threshold value of 4.0 ng/ml, and 36% at a threshold value of 10 ng/ml. With a threshold value of the PSA/prostate volume ratio of 0.25 ng/(ml x cm3), the positive predictive value was 56% compared with 93% for a threshold value of 0.4 ng/(ml x cm3). CONCLUSION: The ratio PSA/prostate volume is a superior method for the diagnosis of prostatic carcinoma both with regard to its sensitivity and its specificity in patients with absolute PSA values in excess of 4 ng/ml.
Benign prostatic hyperplasia (BPH) is a common condition among elderly men. Transurethral needle ablation of the prostate (TUNA) is a minimally invasive procedure for treatment of BPH. With TUNA, the inner region of the prostate is selectively ablated with temperatures approaching 90-100 degrees C while prostatic urothelium is preserved. The TUNA (Precision Plus) was used in 9 patients with BPH: 1 patient had acute urinary retention, 6 ones had suprapubic catheter and 2 patients had lateral and median lobes. The patient with acute urinary retention and 4 patients with suprapubic catheter resumed voiding after TUNA. Two patients with lateral and median lobes showed improvement of subjective and objective parameters. The size of the prostate did not change one month after TUNA. Thus, TUNA is a safe and effective therapy for treatment of BPH that can be performed with local anaesthesia.
Benign prostatic hyperplasia (BPH) is the most common form of prostate disease in middle-aged and elderly men, and leads to severe impairment later in life. Despite its significant impact on public health, the underlying cause of BPH is yet to be determined. This hypothesis proposes a new causal factor for BPH. Applying concepts of dynamics of fluids to the process of urination it could be stated that a turbulent urinary flow through the passage of the urethra. The turbulent urinary flow in the urethra applies pressure and stretch forces to the surrounding tissue. This stimulus repeated over time and coupled with age-related changes of the urethral tissue could contribute to the development of BPH. In support of this hypothesis, several mechanotransduction studies have shown that vibration and pressure forces applied to different cell tissues can provoke cellular and molecular changes. Another supportive data is the presence of the hyperplasic reaction surrounding the urethra specifically located in the transition zone, the only zone where BPH develops. It is crucial to identify causal factors to understanding the disease and to determine effective primary prevention strategies. Future studies of the dynamics of fluids in the urethra are warranted. The finding of significant forces transmitted to the periurethral tissue from a turbulent urinary flow could give us the clue to the underlying cause of BPH. If this hypothesis proves to be valid there are several primary prevention measures that could be implemented to impede the development of BPH. Educational intervention measures in younger populations to avoid frequent urinary retention and active urination (process of forcing the urine through the urethra at a high velocity) could be considered. Studies of the impact of turbulence in the standing vs. sitting position during urination in men should also be considered.
Benign prostatic hyperplasia (BPH) is a local disturbance in the prostate that may involve an inflammatory infiltrate predominantly composed of activated lymphocytes and macrophages. The activation and proliferative response of T lymphocytes to different mitogenic signals has been analysed in peripheral blood mononuclear cells (PBMC) from 45 patients with BPH and 55 healthy controls. The PBMC obtained from the patients showed a significant specific impairment in proliferation, CD25 expression and IL-2 production in response to stimulation with lectins (phytohaemagglutinin (PHA), concanavalin A (Con A)), that was not corrected by the addition of IL-2 or of phorbol esters (phorbol myristate acetate (PMA)). Also, the CD28 response was defective in patient PBMC. Activation with anti-CD3 or anti-CD2 MoAbs was normal, but the addition of PMA to these stimuli provoked a significant defective response. Only the use of transmembrane stimuli (PMA and ionomycin) elicited responses similar to those found in the control group. The results indicate that peripheral T lymphocytes from BPH patients show a functional impairment that is mainly explained by an alteration of membrane signals (PHA, CD28) and is distal to protein kinase C (PKC) activation.
Benign prostatic hyperplasia (BPH) is the nonmalignant enlargement of the prostate gland caused by increases in number of both epithelial and stromal cells. Clinically, BPH leads to voiding dysfunction, which is most often referred to as lower urinary tract symptoms (LUTS). Historically, the only treatments for LUTS due to BPH were watchful waiting or surgery (transurethral or open prostatectomy). However, over the last 20 years medical therapy has taken a prominent role in the management of BPH. Current medical treatments for BPH include alpha-adrenergic receptor antagonists, inhibitors of the 5-alpha reductase enzyme and various phytotherapies. These agents are generally effective and safe; however, many patients are unable to tolerate the side effects or are refractory to medical management and require surgery. In light of this, many potential new therapies for the treatment of BPH are under development. Some represent a variation of current treatments, whereas others target novel molecular pathways within the prostate. The aim of this review is to examine current pharmacotherapies as well as to highlight emerging drugs that may improve our treatment of patients with LUTS secondary to BPH.
Benign prostatic hyperplasia (BPH) is a disease condition characterized by abnormal prostate growth in conjunction with distinct lower urinary tract symptoms. This paper considers the extent to which the prostatic vascular system contributes to normal prostate growth control as well as whether abnormal blood flow patterns in the aging prostate gland might lead to hypoxia-stimulated prostate growth. This relationship is posited from accumulated research that suggests the prostatic vascular system is a primary androgen action target and other research demonstrating the diverse effects of hypoxia in eliciting cell death or cell growth responses. This hypothesis is further supported by the coincidental clinical finding that the presence of cardiovascular disease conditions are among the general risk factors for the development of BPH, and that cardiovascular-active drugs can be used for the treatment of BPH symptoms. This hypothesis has major implications for our understanding of the etiology of BPH, as well as for the development of new and better treatments for this extremely common condition.